Sleep apnea/hypopnea affects around 5% of the adult U.S. population. Short-term effects consist of complete (apnea) or partial (hypopnea) termination of airflow, decreased oxygen in the blood, increased CO2 in the blood, interrupted sleep, and excessive daytime sleepiness. Long-term effects may include hypertension, diabetes, heart attack, stroke, arrhythmia and brain damage.
The principal forms of sleep apnea are: 1) obstructive sleep apnea (OSA), characterized by a physical blockage of the upper airway during sleep, 2) central sleep apnea (CSA), caused by a decreased central respiratory drive during sleep, and 3) mixed sleep apnea, which includes components of both OSA and CSA. OSA is the most common and dangerous of all sleep-related breathing disorders. While CSA is uncommon in its pure form, it is prevalent in patients with congestive heart failure, as a component of Cheyne-Stokes respiration.
The obstructive component in OSA is related to decreased tone in the upper airway as the muscles relax during sleep. In the flaccid airway, muscle tone is insufficient to overcome the combined forces of gravity, surrounding tissue, and the vacuum created by inspiration. Together, these forces act to reduce the cross-sectional area of the airway, decreasing or eliminating airflow.
The treatment of choice for sleep apnea is continuous positive air pressure (CPAP). Basically, CPAP maintains an open airway by inflating it with pressurized air through a nose or face mask. Used properly, CPAP is 100% effective for treating OSA. Although CSA has a neurological origin, it has also been successfully treated with positive air pressure. Despite its efficacy, however, CPAP treatment is poorly tolerated by sleep apnea patients. In one recent survey, CPAP non-compliance (less than 4 h/night) was reported in between 46% and 83% of patients (Weaver and Grunstein, 2008). Reasons for non-compliance include discomfort, claustrophobia, pressure sores, dry nose or mouth, and machine noise.
The most common alternative to CPAP is a surgical removal of the uvula, caudal soft palate, and tonsils. This procedure has a success rate of about 50%. Other surgical treatments, such as tongue reduction, advancement of the tongue, tracheostomy, or implants to stiffen the soft palate have had limited benefit relative to their invasiveness, risk, and irreversibility. Non-surgical approaches such as weight loss, medication, changes in sleeping position or dental appliances also suffer from limited effectiveness or compliance.
Certain implantable medical devices for detecting and/or treat sleep apnea are under investigation but not yet mature. These devices are similar in general design to cardiac pacemakers. With regard to detection, implantable devices have been described that detect apnea by monitoring certain biological signals indicative of respiratory activity, for example, the bioelectric activity of the diaphragm, intercostal muscles, or their efferent nerves, or the bioelectric activity of upper airway muscles or their efferent nerves. Implantable sensors of thoracic pressure and of blood oxygenation are known. With regard to treatment, implantable devices have been described that terminate apnea using drug delivery, atrial overdrive pacing or electrical stimulation of the nerves or muscles that control respiratory activities. Apnea treatments and devices involving delivery of other types of therapeutic response have not been well explored and may provide useful alternatives.